Recurrent ocular herpes simplex virus (HSV) infection of the corneal stroma is one of the leading causes of blindness in this country. The accompanying inflammation seen in ocular HSV infection, the result of interactions between viruses and the immune response, can be both beneficial and potentially harmful to the host. The long term goal of our research is to achieve an understanding of the following: 1) the immunologic and immunopathologic mechanisms of corneal inflammatory disease initiated by interaction of virus and immune cell; 2) the immunologic mechanisms in recovery from the disease: and 3) the host's humoral and cellular immune status during chronic disease, virus persistence (latency), or during recurrent episodes of infection. Information obtained from the assessment of the role of humoral and cellular immune responses in recovery from disease and in recurrent disease may provide new approaches to the management of ocular HSV infections. The mechanism of corneal inflammation in HSV keratitis will be investigated by studies on: 1) antibody in modulating corneal inflammation; 2) corneal hypersensitivity in ocular HSV infection; 3) cell-mediated immunity (CMI) in the recovery from HSV infection; 4) monocyte/macrophage in restricting spread of HSV ocular infection; 5) lymphocytes in supporting the growth of HSV; 6) autosensitization in the pathogenesis of recurrent HSV keratitis and uveitis; 7) CMI in recurrent HSV infection; 8) steroids in potentiating epithelial HSV keratitis; 9) the role of corneal endothelium in supporting the growth of HSV; 10) CMI in recurrent human HSV infection; and 11) hypersensitivity in human corneal inflammation and herpes disciform keratitis. The significance of these studies is the acquisition of information on the pathogenesis of HSV inflammatory disease which will result in a more effective and rational approach for treatment of the infection.